ライフサイエンスコーパス: sorafenib

1 ib and 23 [14%] of 170 patients treated with sorafenib).

2 resistance and limits the clinical impact of sorafenib.

3 ater, and had previously received first-line sorafenib.

4 n strategy to improve the response of CCA to sorafenib.

5 ction was reported in 24% of participants on sorafenib.

6 ular carcinoma (HCC) previously treated with sorafenib.

7 CC cells toward the conventional therapeutic sorafenib.

8 patient profile in the improved response to sorafenib.

9 mutation responsive to targeted therapy with sorafenib.

10 s submitted cases of complete response under sorafenib.

11 of either its parent compound, amonafide, or sorafenib.

12 hepatocellular and renal cell carcinoma drug sorafenib.

13 MEK/ERK signaling, including regorafenib and sorafenib.

14 1% of patients with HCC who are treated with sorafenib.

15 tionally designed combination therapies with sorafenib.

16 r HBV and positive for HCV when treated with sorafenib.

17 connection with the immunological profile of sorafenib.

18 th as a single agent and in combination with sorafenib.

19 ical use, including imatinib, sunitinib, and sorafenib.

20 of the clinically approved kinase inhibitor, sorafenib.

21 fied SLC22A20 (OAT6) as an uptake carrier of sorafenib.

22 fit from treatment with the kinase inhibitor sorafenib.

23 sustained treatment with the FLT3 inhibitor sorafenib.

24 with tivozanib and in 17 (10%) patients with sorafenib.

25 eceived previous treatment with tivozanib or sorafenib.

26 after HCT derive the strongest benefit from sorafenib.

27 least 400 ng/mL who had previously received sorafenib.

28 survival in patients with mRCC treated with sorafenib.

29 and 6 mg/kg, 3 and 6 mg/kg/h for 1 h, i.v.), sorafenib (10 and 20 mg/kg, 10 and 20 mg kg/h for 1 h, i

30 ot followed by sorafenib, was noninferior to sorafenib (10.2 and 9.2 mo [hazard ratio, 0.91; 95% conf

31 igned to receive tivozanib (175 patients) or sorafenib (175 patients).

32 nib (5.6 months, 95% CI 5.29-7.33) than with sorafenib (3.9 months, 3.71-5.55; hazard ratio 0.73, 95%

33 1.5 mg orally once daily in 4-week cycles or sorafenib 400 mg orally twice daily continuously.

34 ed minimisation algorithm to continuous oral sorafenib (400 mg twice-daily) or matching placebo combi

35 patient intolerance to sunitinib (37.5 mg), sorafenib (400 mg) daily, or equivalent placebo with man

36 while 48 patients (22.3%) were treated with sorafenib, 42 patients (19.5%) with TACE and 23 patients

37 ceived 1 year of adjuvant sunitinib (50 mg), sorafenib (800 mg) daily, or equivalent placebo.

38 who were prescribed standard starting dosage sorafenib (800 mg/d per os) versus that of patients who

39 Sorafenib, a multikinase inhibitor approved for the trea

40 idered the principal mechanisms of action of sorafenib, a multitarget kinase inhibitor approved for t

41 antifolate drug, sensitizes cancer cells to sorafenib, a targeted therapy for HCC.

42 Higher (11)C-sorafenib accumulation in tumors at baseline and day 14

43 g of an oncology drug library, we found that sorafenib activates recruitment of the ubiquitin E3 liga

44 c reactions, and seven patients discontinued sorafenib after achieving complete response due to adver

45 randomized, double-blind, three-arm trial of sorafenib after surgical excision of primary renal cell

46 ents receiving no intervention or palliative Sorafenib alone (1-y OS of 0%) or Sorafenib with TARE/SB

47 We report that sorafenib also acts through direct immune modulation, in

48 of this study was to evaluate whether (11)C-sorafenib and (15)O-H(2)O PET have potential to predict

49 survival is 12.6 (11.15 to 13.8) months for sorafenib and 10.2 (8.88 to 12.2) months for "other" tre

50 ning patients were randomly assigned: 157 to sorafenib and 156 to placebo.

51 al time (RMST) was 6.81 years for 3 years of sorafenib and 6.82 years for placebo (RMST difference, 0

52 wth was markedly reduced by cotreatment with sorafenib and adenoviral vectors encoding hOCT1 under th

53 Publications dealing with sorafenib and any of its common adverse effects were con

54 for clinically evaluating the combination of sorafenib and Dinaciclib to improve the therapeutic situ

55 ined in additional malignancies treated with sorafenib and in other angiogenesis inhibitors used in m

56 ivity to cabozantinib and the combination of sorafenib and inhibitors of MAP kinase 1 and MAP kinase2

57 Purpose Sorafenib and lenvatinib are oral multikinase inhibitors

58 Combined therapy using both sorafenib and MEAN enhanced tumor growth inhibition over

59 Microdose (11)C-sorafenib and perfusion (15)O-H(2)O dynamic PET scans we

60 arm), and FLT4 rs307826 and VEGFA rs3024987 (sorafenib and placebo arms combined) were associated wit

61 fail or who do not tolerate the sequence of sorafenib and regorafenib.

62 e confirmed previous reports that sunitinib, sorafenib and TNP-470 are teratogenic and demonstrate th

63 or followed by sorafenib, is noninferior to sorafenib and to compare safety profiles for patients wi

64 spective cohort of HCC patients treated with sorafenib and to describe the profile of the patients wh

65 n, local ablation, transarterial therapy, or sorafenib) and overall survival.

66 tients on sunitinib and 95 [15%] patients on sorafenib), and fatigue 110 [18%] patients on sunitinib

67 hemotherapeutic agents, including cisplatin, sorafenib, and 5-fluorouracil.

68 differentially sensitive to regorafenib and sorafenib, and CCA PDXs were also highly sensitive to re

69 of last 28 days of treatment), progressed on sorafenib, and had Child-Pugh A liver function were enro

70 udies suggested that nonclassical targets of sorafenib are important for the propagation of RVFV.

71 s of DeltaPsim and ROS production induced by sorafenib are independent of caspase activities and do n

72 885657, ITGAV rs3816375, and WWOX rs8047917 (sorafenib arm), and FLT4 rs307826 and VEGFA rs3024987 (s

73 results reveal a new mechanism of action for sorafenib as a mitocan and suggest that high Parkin acti

74 erial activity and found the anticancer drug sorafenib as major hit that effectively kills MRSA strai

75 and selective VEGFR inhibitor) with those of sorafenib as third-line or fourth-line therapy in patien

76 ived any systemic anticancer therapy (except sorafenib) as per investigator decision.

77 ontribution to HCC phenotype and response to sorafenib, as well as the mutual modulation of TP53/MDM2

78 Radiological images taken before starting sorafenib, at first control, after starting sorafenib, a

79 sorafenib, at first control, after starting sorafenib, at the time of complete response, and at leas

80 end toward a decreased rate of discontinuing sorafenib because of adverse events.

81 nib cost and were less likely to discontinue sorafenib because of gastrointestinal adverse effects (8

82 Thus, our mechanistic data indicate that sorafenib bypasses central resistance mechanisms through

83 ission electron microscopy demonstrated that sorafenib caused virions to be present inside large vacu

84 Collectively, these data indicate that sorafenib causes a disruption in viral egress by targeti

85 established cancer-related protein kinases, sorafenib causes variable responses among human tumors,

86 to SIRT and 522 of 608 (85.8%) allocated to sorafenib completed the studies without major protocol d

87 ngs, perfusion (15)O-H(2)O PET findings, and sorafenib concentrations after therapeutic dosing with r

88 C-sorafenib PET did not predict intratumoral sorafenib concentrations after therapeutic dosing, but t

89 hether tumor (11)C-sorafenib uptake predicts sorafenib concentrations during therapy in corresponding

90 (11)C-sorafenib PET findings did not predict sorafenib concentrations in tumor biopsy samples during

91 rienced significantly lower total cumulative sorafenib cost and were less likely to discontinue soraf

92 rs307826 and VEGFA rs58159269 led to reduced sorafenib cytotoxicity.

93 the end of treatment; one patient receiving sorafenib died from infectious colitis while on treatmen

94 The initial sorafenib dose was 400 mg twice per day orally, amended

95 Sorafenib down-regulated total FAK, inducing its proteas

96 ith hepatocellular carcinoma (HCC) receiving sorafenib, drug resistance is common.

97 Molecular markers of sorafenib efficacy in patients with metastatic renal cel

98 In vivo cytokine blocking revealed that sorafenib efficacy is abrogated after inhibition of inte

99 n, diarrhea, and hypertension, compared with sorafenib experience in renal or hepatocellular cancer.

100 ve survival in the second-line setting after sorafenib failure.

101 Administration hospitals who were prescribed sorafenib for hepatocellular carcinoma between January 2

102 nce of any improvement in OS attributable to sorafenib for patients positive for HBV and negative for

103 single-agent therapy or in combination with sorafenib for the management of HCC.

104 l was 238.0 days (95% CI 221.0-281.0) in the sorafenib group and 235.0 days (209.0-322.0) in the plac

105 reported in 65 (41%) of 157 patients in the sorafenib group and 50 (32%) of 156 in the placebo group

106 ents were reported in total, 95 (52%) in the sorafenib group and 86 (48%) in the placebo group.

107 were attributed to study drug; three in the sorafenib group and one in the placebo group.

108 nce in progression-free survival between the sorafenib group and the placebo group (hazard ratio [HR]

109 azard ratio (HR) for relapse or death in the sorafenib group versus placebo group was 0.39 (95% CI, 0

110 ere fatigue (29 [18%] of 157 patients in the sorafenib group vs 21 [13%] of 156 patients in the place

111 21 countries, adults with HCC who tolerated sorafenib (>/=400 mg/day for >/=20 of last 28 days of tr

112 ients on sunitinib and 102 [16%] patients on sorafenib), hand-foot syndrome (94 [15%] patients on sun

113 ssessment Randomized Protocol (SHARP) trial, sorafenib has become the standard of care for patients w

114 However, combination approaches to improve sorafenib have failed.

115 ors of improved survival were treatment with sorafenib (hazard ratio [HR], 0.66; 95% confidence inter

116 Purpose Following the Sorafenib Hepatocellular Carcinoma Assessment Randomized

117 , 6.1 years (IQR 1.7-not estimable [NE]) for sorafenib (HR 0.97, 97.5% CI 0.80-1.17, p=0.7184), and 6

118 ebo versus 85.0% (95% CI, 0.70 to 0.93) with sorafenib (HR, 0.256; 95% CI, 0.10 to 0.65; log-rank P =

119 Sorafenib impaired HCC cell proliferation and induced ap

120 We aimed to determine whether TACE with sorafenib improves progression-free survival versus TACE

121 r carcinoma, while the multikinase inhibitor sorafenib improves survival in patients with advanced di

122 the multitargeted tyrosine kinase inhibitor sorafenib, improves outcome after HCT.

123 tion is being compared with standard-of-care sorafenib in a phase 3 trial.

124 nts (10.7%) received treatment with TACE and sorafenib in combination.

125 vival and cost-effectiveness associated with sorafenib in elderly patients with advanced HCC.

126 ate that 1l augments the cytotoxic action of sorafenib in murine hepatocellular carcinoma cells.

127 Results Hazard ratios show improved OS for sorafenib in patients who are both HBV negative and HCV

128 ctive internal radiation therapy (SIRT) over sorafenib in patients with advanced hepatocellular carci

129 The DECISION trial of sorafenib in patients with differentiated thyroid cancer

130 The clinical benefit of sorafenib in patients with hepatocellular carcinoma (HCC

131 vival and was better tolerated compared with sorafenib in patients with metastatic renal cell carcino

132 l therapy for advanced HCC is noninferior to sorafenib in terms of OS and offers a better safety prof

133 e inhibitor, was found to be non-inferior to sorafenib in terms of overall survival (OS), with signif

134 ers and thereby an increased accumulation of sorafenib in the cancer cells.

135 all and progression-free survival rates than sorafenib in unresectable HCC.

136 B overexpression impaired the sensitivity of sorafenib in vitro and in vivo, implying that PTP1B has

137 ary cohort of patients with HCC treated with sorafenib, increased miR-30e-3p circulating levels predi

138 lying that PTP1B has a significant effect on sorafenib-induced apoptosis.

139 More intriguingly, we find that it is sorafenib-induced ROS accumulation that enables TRAIL to

140 atinocytes and explains the basis underlying sorafenib-induced skin toxicity, with important implicat

141 Instead, sorafenib induces rapid dissipation of the mitochondrial

142 We show that sorafenib inhibits the activity of both complex II/III o

143 findings to identify the mechanism by which sorafenib inhibits the release of RVFV virions from the

144 : We report an immunomodulatory mechanism of sorafenib involving MPhi pyroptosis and unleashing of an

145 Sorafenib is a RAF inhibitor approved for several cancer

146 Sorafenib is associated with improved survival in elderl

147 Purpose Sorafenib is currently the only Food and Drug Administra

148 In addition, sorafenib is described as an antiangiogenic drug, but it

149 ents with advanced hepatocellular carcinoma, sorafenib is the only approved drug worldwide, and outco

150 Sorafenib is the only chemotherapeutic approved for trea

151 r carcinoma (HCC), the multikinase inhibitor sorafenib is the only systemic treatment that has been s

152 However, the therapeutic effect of sorafenib is transient, and patients invariably develop

153 Although the multi-tyrosine kinase inhibitor sorafenib is useful in the treatment of several cancers,

154 kinase inhibitors (MKI) in oncology, such as sorafenib, is associated with a cutaneous adverse event

155 OS) with SIRT, as monotherapy or followed by sorafenib, is noninferior to sorafenib and to compare sa

156 Sorafenib leads to clinical benefit in a subgroup of pat

157 chanistically, the antiangiogenic effects of sorafenib led to increased bone marrow hypoxia, which co

158 ts who were prescribed reduced starting dose sorafenib (< 800 mg/d per os).

159 Sorafenib maintenance therapy reduces the risk of relaps

160 mong the most affected ncRNAs, we found that sorafenib mediated the dysregulation of the lncRNAs GAS5

161 s monotherapy or followed by sorafenib, with sorafenib monotherapy among patients with advanced HCC.

162 the multitargeted and FLT3-kinase inhibitor sorafenib (n = 43) or placebo (n = 40 placebo).

163 (n = 42), MK-2206 plus AZD6244 (n = 75), or sorafenib (n = 61).

164 were randomly assigned to sunitinib (n=647), sorafenib (n=649), or placebo (n=647).

165 Sorafenib (Nexavar) is a broad-spectrum multikinase inhi

166 miR-126-3p were involved in the response to sorafenib of different cancer cell types.

167 re is consistent evidence that the effect of sorafenib on OS is dependent on patients' hepatitis stat

168 ved SIRT and 249 of 575 (43.3%) who received sorafenib only (P < 0.01).

169 dichloroacetate reversed chemoresistance to sorafenib or cisplatin in HCC stem cells derived from fo

170 Median DFS was not reached for 3 years of sorafenib or for placebo (hazard ratio, 1.01; 95% CI, 0.

171 d/or bevacizumab, tyrosine kinase inhibitors sorafenib or lenvatinib may be offered as first-line tre

172 Following first-line therapy with sorafenib or lenvatinib, second-line therapy options for

173 e options for appropriate patients following sorafenib or lenvatinib.

174 of low-dose ADE given alone or combined with sorafenib or vorinostat.

175 ine, felodipine, nicardipine, nilotinib, and sorafenib) or low micromolar range (abiratone, candesart

176 afenib for patients who previously tolerated sorafenib, or ramucirumab (for patients with alpha-fetop

177 In addition to sorafenib, other multi-kinase inhibitors have been appro

178 Here we demonstrate that sorafenib overcomes TRAIL resistance in RCC by a mechani

179 tients (63%) and 1,809 reduced starting dose sorafenib patients (37%).

180 Results There were 3,094 standard dose sorafenib patients (63%) and 1,809 reduced starting dose

181 Reduced starting dose sorafenib patients experienced significantly lower total

182 Consequently, reduced starting dose sorafenib patients had lower OS (median, 200 v 233 days,

183 Reduced starting dose sorafenib patients had more Barcelona Clinic Liver Cance

184 eived only one prior VEGFR-targeted therapy (sorafenib, pazopanib, or cediranib), and four patients h

185 Conclusion: Microdose (11)C-sorafenib PET did not predict intratumoral sorafenib con

186 Results: (11)C-sorafenib PET findings did not predict sorafenib concent

187 ncluded determining the association of (11)C-sorafenib PET findings, perfusion (15)O-H(2)O PET findin

188 In addition, sorafenib plasma and tumor concentrations were not assoc

189 of the drugs gilteritinib, quizartinib, and sorafenib predict even wider use of FLT3 inhibitors goin

190 eated or intolerant without viral hepatitis, sorafenib progressor without viral hepatitis, HCV infect

191 vestigate the underlying mechanisms by which sorafenib promotes keratinocyte cytotoxicity and subsequ

192 ases resistance to methionine restriction or sorafenib, promotes epithelial-mesenchymal transition, a

193 Here, we demonstrate that RAF inhibition by sorafenib rapidly leads to RAF dimerization and ERK acti

194 ients on sunitinib and 208 [33%] patients on sorafenib), rash (15 [2%] patients on sunitinib and 95 [

195 ce its approval, for the following 10 years, sorafenib remained the only systemic agent with proven c

196 Sorafenib remains the only approved drug for treating pa

197 s transient, and patients invariably develop sorafenib resistance (SR).

198 Depletion of METTL3 under hypoxia promotes sorafenib resistance and expression of angiogenesis gene

199 This study unveils a novel mechanism of sorafenib resistance depending on the alpha3beta1/Ln-332

200 els of miR-30e-3p predict the development of sorafenib resistance in a preliminary series of patients

201 sis inhibitor, to reverse tumorigenicity and sorafenib resistance mediated by PRMT6 deficiency in HCC

202 els, METTL3 depletion significantly enhances sorafenib resistance of HCC by abolishing the identified

203 ide a mechanistic link among tumorigenicity, sorafenib resistance, and glucose metabolism.

204 n of the Tec family kinase BMX occurs during sorafenib resistance.

205 urine FLT3-ITD-positive (FLT3-ITD+) model of sorafenib resistance.

206 Federal Drug Administration as an option for sorafenib-resistant advanced hepatocellular carcinoma, i

207 nes, as well as of blasts from patients with sorafenib-resistant AML, suggested an enrichment of the

208 esses the growth of high-FGFR-expressing and sorafenib-resistant HCCs.

209 se, is significantly down-regulated in human sorafenib-resistant hepatocellular carcinoma (HCC).

210 3 expression in both sorafenib-sensitive and sorafenib-resistant Huh-7 cells, inhibiting TYRO3/growth

211 tudy, we generated two functionally distinct sorafenib-resistant human Huh-7 HCC cell lines in order

212 ndidates were suggested for the selection of sorafenib-responding patients.

213 represents an effective approach to improve sorafenib response and to prevent sorafenib treatment es

214 a promising combination strategy to improve sorafenib response in HCC.

215 els could make tumor cells more sensitive to sorafenib's actions, providing one possible explanation

216 HSC-CM or Ln-332 inhibited sorafenib's effectiveness in HCC cells expressing both a

217 y was to investigate the effect of Ln-332 on sorafenib's effectiveness.

218 ffectively silenced TYRO3 expression in both sorafenib-sensitive and sorafenib-resistant Huh-7 cells,

219 xpression of FOXO3 restores m(6) A-dependent sorafenib sensitivity.

220 Sorafenib should not be used as adjuvant therapy for RCC

221 While FLT3 inhibitors like sorafenib show initial therapeutic efficacy, resistance

222 novel ARAF positive mutation, treatment with sorafenib showed regression of the choroidal lesions and

223 Sorafenib (SOR) is currently used for hepatocellular car

224 IRT (SIRveNIB and SARAH) or SIRT followed by sorafenib (SORAMIC), were included.

225 E), for oral delivery of a hydrophobic drug, sorafenib (SRF).

226 There are few data examining how sorafenib starting dose may influence patient outcomes a

227 Mechanism-of-action studies indicated that sorafenib targeted a late stage in virus infection and c

228 rch is in identifying the cellular target of sorafenib that inhibits RVFV propagation, so that this i

229 ry limited survival benefits with the use of sorafenib, the current standard of care for advanced dis

230 Sorafenib, the first and only targeted drug approved for

231 ious in inhibiting tumor growth in mice than sorafenib, the only approved drug for HCC.

232 cts lethal autophagy in HCC cells induced by sorafenib, the standard of care for advanced HCC patient

233 Conclusion The initiation of sorafenib therapy at reduced dosages was associated with

234 th hepatocellular carcinoma in whom previous sorafenib therapy had failed.

235 er "paradoxical" ERK activation occurs after sorafenib therapy in HCC, and if so, if it impacts the t

236 ) A modification in the resistance of HCC to sorafenib therapy.

237 cans were performed before and after 2 wk of sorafenib therapy.

238 INTERPRETATION: The addition of sorafenib to DEB-TACE does not improve progression-free

239 This study highlighted the capability of sorafenib to modulate the expression of a wide range of

240 as no additional prognostic effect of adding sorafenib to TACE treatment in this patient cohort.

241 ctiveness ratios (ICERs) were calculated for sorafenib-treated and control patients.

242 nel of lncRNAs and miRNAs by qPCR array in a sorafenib-treated hepatocellular carcinoma (HCC) cell li

243 Caspase 1 analysis in sorafenib-treated MPhi revealed an induction of pyroptos

244 cells become activated when cocultured with sorafenib-treated MPhi, leading to tumor cell death.

245 We included 228 sorafenib-treated patients and 870 control patients.

246 The median survival of the sorafenib-treated patients was 150.5 days versus 62 days

247 n in VEGFA and FLT4 could affect survival in sorafenib-treated patients with mRCC.

248 She was commenced on sorafenib treatment but required early dose reductions d

249 ility of dual RAF/MEK inhibition to overcome sorafenib treatment escape in HCC.

250 to improve sorafenib response and to prevent sorafenib treatment escape in HCC.

251 th hepatocellular carcinoma in whom previous sorafenib treatment had failed.

252 mall number of cases of complete response to sorafenib treatment have now been reported worldwide, ho

253 ciated HCC can attain excellent responses to sorafenib treatment that is durable.

254 one, which activates the mitophagy response, sorafenib treatment triggers PINK1/Parkin-dependent cell

255 Previous sorafenib treatment was allowed.

256 ced solid malignancies and an indication for sorafenib treatment were included.

257 patients with HCC who have progressed during sorafenib treatment.

258 vival benefit in HCC patients progressing on sorafenib treatment.

259 oemoblisation treatment and was commenced on sorafenib treatment.

260 cinoma (HCC) whose disease progresses during sorafenib treatment.

261 imaging revealed progressive disease despite sorafenib treatment.

262 vival benefit in HCC patients progressing on sorafenib treatment.

263 ainst IGF1 and IGF2 (xentuzumab), along with sorafenib; tumor growth was measured and tissues were an

264 We tested sunitinib and sorafenib, two oral anti-angiogenic agents that are effe

265 expansion phase to patients in four cohorts: sorafenib untreated or intolerant without viral hepatiti

266 and iCCA (HuCCT1) cells with hOCT1 enhanced sorafenib uptake and cytotoxic effects.

267 sion: The reason for impaired hOCT1-mediated sorafenib uptake by CCA is multifactorial.

268 objective was to assess whether tumor (11)C-sorafenib uptake predicts sorafenib concentrations durin

269 tor) restored hOCT1 expression and increased sorafenib uptake.

270 rOct1 expression was accompanied by impaired sorafenib uptake.

271 ting (HR, 1.45; 95% CI, 1.21-1.73.) Although sorafenib use was associated with a survival benefit (HR

272 therapy was 120.0 days (IQR 43.0-266.0) for sorafenib versus 162.0 days (70.0-323.5) for placebo.

273 dian daily dose was 660 mg (IQR 389.2-800.0) sorafenib versus 800 mg (758.2-800.0) placebo, and media

274 ase-free survival (DFS) comparing 3 years of sorafenib versus placebo.

275 ial radioembolization with yttrium 90 in the Sorafenib versus Radioembolization in Advanced Hepatocel

276 igh-risk patients randomized to sunitinib or sorafenib vs placebo among patients with stages comparab

277 ) in the ASSURE trial (adjuvant sunitinib or sorafenib vs placebo in resected unfavorable renal cell

278 es in the study groups) with those receiving sorafenib was calculated.

279 Sorafenib was confirmed to inhibit MAPK signaling in the

280 In addition, sorafenib was found to down-regulate major histocompatib

281 s implanted in mouse liver, poor response to sorafenib was observed.

282 large prospective randomized trials in which sorafenib was the control arm.

283 the secretory pathway and a known target of sorafenib, was found to be important for RVFV egress.

284 ian OS with SIRT, whether or not followed by sorafenib, was noninferior to sorafenib (10.2 and 9.2 mo

285 of the oral antitumor multikinase inhibitor sorafenib, we profiled the expression of a panel of lncR

286 les of these patients receiving sunitinib or sorafenib were also performed.

287 of 3,256 patients, 1,643 (50%) who received sorafenib were available.

288 t TACE and a combination therapy of TACE and sorafenib were significant prognostic factors in metasta

289 more previous systemic therapies, including sorafenib, were randomly assigned to receive 30 mg/m(2)

290 the rate of occurrence of adverse effects of sorafenib when used in differentiated thyroid cancer com

291 le, except for fluticasone, nicardipine, and sorafenib which suffer from severe matrix suppression.

292 sma membrane was driven by the RAF inhibitor sorafenib, which increases the affinity of Ras-GTP:RAF1

293 tment is the multi-tyrosine kinase inhibitor sorafenib, which shows low response rates and severe sid

294 resented in terms of hazard ratios comparing sorafenib with alternative therapies according to hepati

295 Combination of sorafenib with Cdk5 inhibition (genetic knockdown by sho

296 trials, involving 1,243 patients, comparing sorafenib with SIRT (SIRveNIB and SARAH) or SIRT followe

297 palliative Sorafenib alone (1-y OS of 0%) or Sorafenib with TARE/SBRT (2-y OS of 17%) at our center d

298 d CXCR4-targeted nanoparticles to co-deliver sorafenib with the MEK inhibitor AZD6244 in HCC.

299 omparing SIRT, as monotherapy or followed by sorafenib, with sorafenib monotherapy among patients wit

300 mmittee on Cancer stage III/IV) who received sorafenib within 6 months of diagnosis (and were otherwi